Plumbism | definition of plumbism by Medical dictionary Plumbism | definition of plumbism by Medical dictionary Related to plumbism: lead poisoning lead1 (Pb) [led] a chemical element, atomic number 82, atomic weight 207.19. Excessive ingestion or absorption causes lead poisoning . (See also Appendix 6.) l. poisoning poisoning caused by the presence of lead or lead salts in the body; it affects the brain, nervous system, blood, and digestive system and can be either chronic or acute. Called also plumbism and saturnism . Chronic Lead Poisoning. This was once fairly common among painters, and was called “painter's colic.” It became less frequent as lead-free paints were substituted for lead-based ones and as plastic toys replaced lead ones. The disease is still seen among children with pica (a craving for unnatural articles of food) who may eat lead paint chips or coatings. The Centers for Disease Control and Prevention defines an elevated blood lead level as &gt;10 μg/dL for children younger than six years of age.

However, there is evidence that there are subtle effects even at lower levels Symptoms include weight loss, anemia, stomach cramps (lead colic), a bluish black line at the edge of the gums, and constipation. Other symptoms may be mental depression and, in children, irritability and convulsions. In addition to the poisoning, the anemia and weight loss must also be treated, usually by providing an adequate diet. In serious cases, EDTA (calcium disodium edetate) may be prescribed. Acute Lead Poisoning. This rare condition can be caused in two ways: lead may accumulate in the bones, liver, kidneys, brain, and muscles and then be released suddenly to produce an acute condition; or large amounts of lead may be inhaled or ingested at one time. Symptoms are a metallic taste in the mouth, vomiting, bloody or black diarrhea, and muscle cramps. Diagnosis is made by examination of the blood and urine. Treatment. Immediate removal of unabsorbed lead in the intestinal tract through the administration of mild saline cathartics and enemas. EDTA is given and in most cases measures must be taken to reduce the increased intracranial pressure that accompanies acute lead poisoning. Prevention.

An awareness of the prevalence of lead poisoning among children of preschool age who live in poorly maintained housing has led to neighborhood screening surveys in high-risk areas. An important aspect of prevention of lead poisoning is determination of sources of lead in the environment and efforts to remove them. Sources include peeling paint from window sills, walls, floors, and bannisters, and from soil around old houses that have shed exterior paint through the years. An often unsuspected source is the glaze of certain pottery and “leaded glass;” lead can leach out into food and beverages from such vessels. A vital factor in coping with the problem of lead contamination is public education and development of a community awareness of possible sources and of the need for elimination of these hazards from the environment.

lead poi·son·ing acute or chronic intoxication by lead or any of its salts; symptoms of acute lead poisoning usually are those of acute gastroenteritis in adults or encephalopathy in children; chronic lead poisoning is manifested chiefly by anemia, constipation, colicky abdominal pain, neuropathy with paralysis with wrist-drop involving the extensor muscles of the forearm, bluish lead line of the gums, and interstitial nephritis; saturnine gout, convulsions, and coma may occur. plumbism - Memidex dictionary/thesaurus plumbism toxic condition produced by the absorption of excessive lead into the system Class: Wikipedia: Lead poisoning | plumbism | colica Pictonum | saturnism | painter's colic a medical condition in humans and other vertebrates caused by increased levels of the heavy metal lead in the body. Lead interferes with a variety of body processes and is toxic to many organs and tissues including the heart, bones, intestines,...

SYMPTOMS OF LEAD POISONING IN ADULTS - POISONING IN ADULTS - SILENT REFLUX SYMPTOMS SYMPTOMS OF LEAD POISONING IN ADULTS - POISONING IN ADULTS SYMPTOMS OF LEAD POISONING IN ADULTS - POISONING IN ADULTS Symptoms of lead poisoning in adults - Period symptoms no bleeding Symptoms Of Lead Poisoning In Adults lead poisoning Lead poisoning (also known as plumbism, colica Pictonum, saturnism, Devon colic, or painter's colic) is a medical condition caused by increased levels of the heavy metal lead in the body. poisoning caused by the absorption of excess lead into the body; it can result in anemia; in young children the body tends to deposit excess amounts of lead in brain tissue where it can result in limitation of brain development and impaired cognitive development Acute or chronic poisoning due to the absorption of lead into the body toxic condition produced by the absorption of excessive lead into the system in adults Voice therapy programs generally include education about voice and training in technical skills. Within the educational component, two basic topics are covered.

symptoms A physical or mental feature that is regarded as indicating a condition of disease, particularly such a feature that is apparent to the patient A sign of the existence of something, esp. of an undesirable situation (symptom) anything that accompanies X and is regarded as an indication of X's existence (symptom) (medicine) any sensation or change in bodily function that is experienced by a patient and is associated with a particular disease Symptoms is a 1974 British horror film directed by José Ramón Larraz. It was entered into the 1974 Cannes Film Festival. Although circulated privately through bootlegs, the original prints are missing, and was last show on British television in 1983. symptoms of lead poisoning in adults - 9 WAYS 9 WAYS YOU GET LEAD POISONING This 20-page report - 9 Ways You Get Lead Poisoning - describes how lead poisoning can happen and helps you protect yourself and your children from the sometimes deadly consequences of lead poisoning. It also points out possible symptoms, how lead poisoning is diagnosed, treatment, the medical and social effects, and what you can do to prevent or minimize exposure to lead.

This 20-page report - 9 Ways You Get Lead Poisoning - describes how lead poisoning can happen and helps you protect yourself and your children from the sometimes deadly consequences of lead poisoning. It also points out possible symptoms, how lead poisoning is diagnosed, treatment, the medical and social effects, and what you can do to prevent or minimize exposure to lead. 75% (10) Castor Bean fruit - ricinus communis The castor oil plant, Ricinus communis, is a plant species of the Euphorbiaceae. Its seed is the castor bean which, despite its name, is not a true bean.Castor seed is the source of castor oil, which has a wide variety of uses. The seeds contain between 40% and 60% oil that is rich in triglycerides, mainly ricinolein. The seed coat contains ricin, a poison, which is also present in lower concentrations throughout the plant. The toxicity of raw castor beans is well-known, and reports of actual poisoning are relatively rare. Children could conceivably die from as few as three beans; adults may require eight or more.

As an example of the rarity of castor bean poisoning, in recent years there have only been two cases reported in all of England, and both the victims recovered uneventfully. Castor oil plant From Wikipedia, the free encyclopedia (Redirected from Castor bean) Jump to: navigation, search Castor oil plant Castor bean in disturbed area Scientific classification Kingdom: Plantae Phylum: Magnoliophyta Class: Magnoliopsida Order: Malpighiales Family: Euphorbiaceae Subfamily: Acalyphoideae Tribe: Acalypheae Subtribe: Ricininae Genus: Ricinus Species: R. communis Binomial name Ricinus communis L. The castor oil plant, Ricinus communis, is a plant species of the Euphorbiaceae (the evolution of this plant family is relatively unexplored [1]) the sole member of the genus Ricinus and of the subtribe Ricininae. Its seed is the castor bean which, despite its name, is not a true bean. Castor seed is the source of castor oil, which has a wide variety of uses.

The seeds contain between 40% and 60% oil that is rich in triglycerides, mainly ricinolein. The seed coat contains ricin, a poison, which is also present in lower concentrations throughout the plant. The toxicity of raw castor beans is well-known, and reports of actual poisoning are relatively rare. Children could conceivably die from as few as three beans; adults may require eight or more. As an example of the rarity of castor bean poisoning, in recent years there have only been two cases reported in all of England, and both the victims recovered uneventfully.[1] Even so small a dose of ricin as 1/25 000 000 of the body weight may cause toxic symptoms when injected. [2] Castor seeds have been found in Egyptian tombs dating back to 4000 BC. Herodotus and other Greek travelers have noted the use of castor seed oil for lighting, body ointments, and improving hair growth and texture. Cleopatra is reputed to have used it to brighten the whites of her eyes.

The Ebers Papyrus is an ancient Egyptian medical treatise believed to date from 1552 BC. Translated in 1872, it describes castor oil as a purgative. Global castor seed production is around 1 million tons per year. Leading producing areas are India (with over 60% of the global yield), China and Brazil. There are several active breeding programmes. Another plant species, Fatsia Japonica, looks similar to the castor oil plant and is known as the false castor oil plant. Contents [hide] 1 Description 2 Nomenclature 3 Habitat and growth 4 Plant-animal interactions 5 Uses 6 Production 7 Gallery 8 Common Names 9 References 10 Further reading 11 See also 12 External links [edit] Description Castor oil plant can reach a height of 2–3 m in a year (if sown early, under glass, and kept at a temperature of around 20°Celsius/68°Fahreheit until planted out [2]).

The glossy leaves are 15–45 cm long, long-stalked, alternate and palmate with 5–12 deep lobes with coarsely toothed segments. Their colour varies from dark green, sometimes with a reddish tinge, to dark reddish purple or bronze. The stems and the spherical, spiny seed pods also vary in pigmentation. The pods are more showy than the flowers (the male flowers are yellowish-green with prominent creamy stamens and are carried in ovoid spikes up to 15 cm long; the female flowers, borne at the tips of the spikes, have prominent red stigmas). [3] Terminating stems are panicle-like inflorescences of green monoecious flowers, the stalked female flowers above the male flowers below, both without petals. The fruit is a spiny, greenish capsule with large, oval, shiny, bean-like, highly poisonous seeds with variable brownish motling. [edit] Nomenclature The name Ricinus is a Latin word for tick; the seed is so named because it has markings and a bump at the end which resemble certain ticks.

The common name "castor oil" likely comes from its use as a replacement for castoreum, a perfume base made from the dried perineal glands of the beaver (castor in Latin). It has another common name, Palm of Christ, or Palma Christi, that derives from castor oil's ability to heal wounds and cure ailments. Elizabeth Park Herb Garden - Hartford/ West Hartford DSCN5726 Blue-ringed Octopus Profile Mad About Us 3: Blue-ringed Octopus The blue-ringed octopuses (genus Hapalochlaena) are three (or perhaps four) octopus species that live in tide pools in the Pacific Ocean, from Japan to Australia. Despite their small size and relatively docile nature, they are currently recognized as one of the world's most venomous animals. They are recognized by their characteristic blue and black rings and yellowish skin. It hunts small crabs, hermit crabs, and shrimp, and may bite attackers, including humans, if provoked or stepped on. The genus was described by British zoologist Guy Coburn Robson in 1929.

There are three confirmed species of Hapalochlaena, and a fourth is still under research: Greater Blue-ringed Octopus (Hapalochlaena lunulata) Southern Blue-ringed Octopus or Lesser Blue-ringed Octopus (Hapalochlaena maculosa) Blue-lined Octopus (Hapalochlaena fasciata) ?Hapalochlaena nierstraszi - described in 1938 from a single specimen from the Bay of Bengal; the validity of this taxon has been questioned. An individual blue-ringed octopus tends to use its dermal chromatophore cells to camouflage itself until provoked, at which point it quickly changes color, becoming bright yellow with blue rings or lines. Feeding Their diet typically consists of small crab and shrimp, but they may also feed on fish if they can catch them. They pounce on their prey, paralyze them with venom and use their beaks to tear off pieces. They then suck out the flesh from the crustacean's exoskeleton. In laboratory conditions they have been observed to engage in cannibalism, however this has not been recorded in the wild.

Breeding A male mates with a female by grabbing her mantle, which sometimes completely obscures the female's vision, then transferring sperm packets by inserting his hectocotylus into her mantle cavity over and over again. Mating continues until the female has had enough, and in at least one species the female has to remove the over-enthusiastic male by force. Males will attempt copulation with members of their own species regardless of sex or size, however interactions between males are most often shorter in duration and end with the mounting octopus withdrawing the hectocotylus without packet insertion or struggle. Blue-ringed octopus females lay only one clutch of about fifty eggs in their lifetime towards the end of Autumn. Eggs are laid then incubated underneath the female's arms for approximately six months, and during this process she will not eat. After the eggs hatch, the female dies, and the new offspring will reach maturity and be able to mate by the next year. Venom Blue-ringed octopus from New South Wales, Australia The blue-ringed octopus is the size of a golf ball, but its venom is powerful enough to kill humans. There is no blue-ringed octopus antivenin available.

The octopus produces venom that contains tetrodotoxin, 5-hydroxytryptamine, hyaluronidase, tyramine, histamine, tryptamine, octopamine, taurine, acetylcholine, and dopamine. The major neurotoxin component of blue-ringed octopus venom was originally known as maculotoxin but was later found to be identical to tetrodotoxin, a neurotoxin which is also found in pufferfish and cone snails. Tetrodotoxin blocks sodium channels, causing motor paralysis and sometimes respiratory arrest leading to cardiac arrest due to a lack of oxygen. The toxin is created by bacteria in the salivary glands of the octopus. Treatment First aid treatment is pressure on the wound and rescue breathing. It is essential, if rescue breathing is required, that it be continued until the victim begins to breathe, which may be some hours. Hospital treatment involves respiratory assistance until the toxin is washed out of the body. The symptoms vary in severity, with children being the most at risk because of their small body size. The victim might be saved if artificial respiration starts before marked cyanosis and hypotension develop.

Victims who live through the first 24 hours generally go on to make a complete recovery. It is essential that immediate and full-time respiratory support be given (e.g., artificial respiration/rescue breathing) even if the victim appears not to be responding. Tetrodotoxin poisoning can result in the victim being fully aware of his surroundings but unable to breathe. Because of the paralysis that occurs they have no way of signalling for help or any way of indicating distress. Respiratory support, together with reassurance, until medical assistance arrives ensures that the victim will generally recover well. The blue-ringed octopus is currently one of the most dangerous known sea creatures and, despite its small size, the blue-ringed octopus carries enough venom to kill 26 adult humans within minutes. symptoms of lead poisoning in adults Lead heavy metal home test kit tests the presence of ions of Lead to a high degree of accuracy to detect contamination in the body and on a wide range of materials in your environment. Very simple to use & designed specifically for homeowner/consumer use only. Lead toxicity at home test kit will test as well as water and tell you the approx. lead release in the sample.

Test in the privacy of your own home, office or work with no cost-prohibitive lab fees or long wait times. Lead poisoning test kit detects lead instantly at-home with no sending samples to costly labs. Get results instantly at-home. cardiovascular effects reproductive toxicity Humans have been mining and using this heavy metal for thousands of years, poisoning themselves in the process due to accumulation and exposure. These dangers have long been known, though the modern understanding of their full extent and the small amount of lead necessary to produce them is relatively recent; blood lead levels once considered safe are now considered hazardous, with no known threshold. Description of the Disease of Lead Poisoning Lead is primarily ingested or inhaled. The most common source of lead exposure is ingestion of lead containing dust. The rate of lead uptake is affected by the individual's developmental stage, the route of exposure, and the nature of the lead [compounds] to which the individual is exposed. Nutritional status is also important: a healthy diet high in iron and calcium and low in fat, for example, may slow the rate of lead absorption. According to the Agency for Toxic Substances and Disease Registry (ATSDR), absorption depends on the form of the lead.

Inhaled, airborne lead is almost totally absorbed, while ingested lead absorption rates may vary from 10% in adults to 50% in children. Lead is absorbed more efficiently in dust from sanded lead-based paint than from whole paint chips. The most dangerous exposure is to lead vapors (formed whenever lead is melted) or other inhalable lead compounds. Absorbed lead is detectable in blood, soft tissue and bone. The half-life of lead varies from about one month in blood, 1-1.5 months in soft tissue, to about 25-30 years in bone. As of summer 2012, EBLL or lead poisoning is defined by the CDC as a blood lead level of 5 mcg/dL or greater, which represents the top 2.5% of children whose blood lead levels were tested. This is now the level at which both the CDC and MDH recommend taking action. Lead Poisoning: Acute and Chronic Disease The disease of lead poisoning can be divided into acute disease referring to current EBLLs and chronic disease referring to the cumulative effects of EBLLs on the body lead level.

In both acute and chronic disease the most prominent signs and symptoms are neurological-for children this may lead to permanent neurological effects. Children with very high BLLs (≥60 mcg /dL) should be treated as medical emergencies, regardless of whether or not the child displays symptoms. Ingestion of a metallic object that may contain lead can result in an EBLL within hours. Any child that has ingested a metallic object that may contain lead should receive immediate medical attention including a blood lead test and abdominal x-ray. Lead Poisoning: Acute Disease Acute exposure to lead generally means exposure for a short time, but at high levels. The following are symptoms of acute exposure but are seldom caused by EBLLs <50 mcg/dL. most common = intermittent abdominal pain constipation or diarrhea These symptoms may be warnings of even more serious symptoms to follow: seizures coma possibly death The EBLLs associated with encephalopathy in children vary from study to study, but BLLs of 70-80 mcg/dL or greater appear to indicate a serious risk (ATSDR 2010).

An example of acute disease occurred in 2006 A Minnesota child died as a result of swallowing a lead-containing bracelet that came with a pair of shoes. This case study can be found at: (PDF) Lead Poisoning: Chronic Disease Chronic lead exposure generally means exposure to low to moderate levels of lead over a long period of time. Recent studies confirm that lead absorption is harmful at any concentration. Relatively low blood lead levels rarely cause noticeable signs and symptoms, but can cause permanent damage-especially in young children-including but not limited to: decreased IQ ADHD other behavioral disturbances. A study of US adolescents published in the Archives of Internal Medicine, in January 2010 not only showed that there were long lasting effects of lead poisoning (decreased kidney function) but that these effects were noted in adolescents whose EBLLs were less than 10 mcg/Dl (Fadrowski et al, 2010). Due to the numerous adverse effects of EBLLs, the government requires that blood lead testing be done at 12 and again at 24 months for children enrolled in MA or MinnesotaCare. The following web page provides additional resources for lead in English and Spanish as well as other lead related information.

Sources of Lead in the Environment Paint Lead was used in common house paint until 1978 when the Consumer Product Safety Commission (CPSC) restricted its use in household paint. Many buildings built before 1978 have lead-based paint inside and outside. Housing built before 1950 is at even greater risk of having interior lead-based paint, the older the building, the more likely it is to contain lead paint. Chipping, peeling or chalking lead paint is a common source of ingestible lead dust and creates a strong potential for lead exposure. Dust Lead paint dust is the most common source of lead exposure for children. Lead as dust is much more easily absorbed. Interior house dust can become contaminated with lead as the result of the deterioration or disturbance of leaded paint. Fine lead dust, and resulting contamination, can be created when painted surfaces rub against each other, such as where double hung windows slide up and down or when doors open and close. Lead in dust is increased after older paint has been disturbed through remodeling, renovation or repainting. Additionally, people track in contaminated soil on their shoes and/or clothing, and the fallout of airborne lead particles from industrial or vehicular sources and can create contaminated dust.

Occupational Exposures or "Secondary Transmission" Household contacts of persons with occupational, vocational, or other exposures may be exposed to lead dust or other compounds brought in to the home. Some of the occupations that carry a potential for exposure to lead include: building demolition radiator repair bridge construction People who work in a lead environment may bring lead dust into their car or home on their clothes and bodies and unintentionally expose their family. Proper hygiene practices such as washing or showering and changing out of work clothes before leaving for home will eliminate or at the least substantially decrease the amount of lead dust brought into the home. Folk Medicines and Cosmetics Many home remedies popular in some ethnic communities may contain lead. Medications may be as much as 90% lead by weight and include: Greta, Alarcon, Rueda and Azarcon, used for gastro-intestinal disturbances in the Latino community (empacho) "Pay-loo-ah," used by many Southeast Asians.

Cosmetic products are a primary source of lead in Asian and Arab countries Applying Kohl results in lead exposure primarily via hand-to-eye-to-mouth activities and subsequent ingestion of particles Hobby Sources Many hobbies involve lead use such as: making or handling lead buckshot/bullets fishing weights/sinkers stained glass solder ceramic glazing Heating and melting lead is particularly dangerous because of the formation of lead vapor, so respirator use and proper ventilation are required to prevent exposure. Other hobbies that carry a potential for exposure to lead include: furniture refinishing painting target shooting at firing ranges Hobbyists can protect their families by keeping the hobby activity away from living areas and by showering or changing clothes before entering the home. Tableware Lead may be found in the following dishes, glasses, and pottery: poorly glazed ceramic dishes and pottery (in particular chipped, Imported, old, or handmade) leaded crystal pewter brass In these pieces, acid substances may interact chemically with the glaze and accelerate the lead release. Therefore, acidic foods (such as orange, tomato and other fruit juices, tomato sauces, wines, and vinegar) stored in improperly glazed containers are potentially the most dangerous.

If it is not known whether or not a particular tableware item contains lead, the item should not be used to store, cook or serve food or beverages. Water Most well or city water does not naturally contain lead although some old well pumps still in operation may have the potential for contaminating the well with lead. In homes where older plumbing has not been updated, lead pipes can be a source of water contamination. Lead leaches into drinking water from these lead pipes as well as brass faucets and lead solder that connects the pipes. Hot water is particularly corrosive and should not be used for drinking, cooking, or preparing infant formula. The cold-water tap should be flushed for several minutes each morning or after sitting until there is a noticeable change in temperature of the water before any water is consumed. Miscellaneous Sources Lead solder is no longer used in the processing of canned foods in the United States dramatically reducing lead in food. However, imported food products may still contain lead as some foreign manufacturers use lead solder in cans. Some imported food products that are sold in ethnic markets, at swap meets, and by door-to-door vendors may contain high levels of lead. Food may also be contaminated with lead from the soil or use of lead-based pesticides in the growing process.

In recent years, lead has been found in candy imported from countries such as Mexico. The lead ink from the paper wrapper contaminates the candy, especially if these products are acidic tamarind and tejocote fruit. There continues to be an ever-increasing array of household products that contain lead, especially imported products. In recent years, lead has been found in: vinyl miniblinds PI-13/PI008: Toxicity of Pesticides Toxicity of Pesticides 1 O. Norman Nesheim, Frederick M. Fishel, and Mark Mossler 2 This document describes how pesticides work on living things, so you can learn to reduce or eliminate human exposure. Background Pesticides are designed to control pests, but they can also be toxic (poisonous) to desirable plants and animals, including humans. Some pesticides are so highly toxic that very small quantities can kill a person, and almost any pesticide can make people ill if they are exposed to a sufficient amount. Because even fairly safe pesticides can irritate the skin, eyes, nose, or mouth, it is a good idea to understand how pesticides can be toxic so you can follow practices designed to reduce or eliminate your exposure and the exposure of others to them.

How Pesticides Enter the Body Before a pesticide can harm you, it must be taken into the body. Pesticides can enter the body orally (through the mouth and digestive system); dermally (through the skin) or by inhalation (through the nose and respiratory system). Oral Exposure Oral exposure may occur because of an accident, but is more likely to occur as the result of carelessness, such as blowing out a plugged nozzle with your mouth, smoking or eating without washing your hands after using a pesticide, splashing concentrate while mixing, or eating fruit that has been recently sprayed with a pesticide containing residues above the tolerance set for the commodity by the Environmental Protection Agency. The seriousness of the exposure depends upon the oral toxicity of the material and the amount swallowed. Dermal Exposure Dermal (skin) exposure accounts for about 90% of the exposure pesticide users receive from nonfumigant pesticides. It may occur any time a pesticide is mixed, applied, or handled, and it often goes undetected. Both liquid pesticides and dry materials—dusts, wettable powders, and granules—can be absorbed through the skin.

The seriousness of dermal exposure depends upon: the dermal toxicity of the pesticide; rate of absorption through the skin; the size of the skin area contaminated; the length of time the material is in contact with the skin; and the amount of pesticide on the skin. Absorption continues to take place on all of the affected skin area as long as the pesticide is in contact with the skin. The seriousness of the exposure is increased if the contaminated area is large or if the material remains on the skin for a period of time. Rates of absorption through the skin are different for different parts of the body. Usually, absorption through the forearm is the standard against which absorption rates in other areas of the body is tested. Absorption is over 11 times faster in the lower groin area than on the forearm (Table 1). Absorption through the skin in the genital area is rapid enough to approximate the effect of injecting the pesticide directly into the bloodstream. Table 1. 100 Inhalation Exposure Inhalation exposure results from breathing pesticide vapors, dust, or spray particles. Like oral and dermal exposure, inhalation exposure is more serious with some pesticides than with others, particularly fumigant pesticides, which form gases.

Inhalation exposure can occur by breathing smoke from burning containers; breathing fumes from pesticides while applying them without protective equipment; and inhaling fumes while mixing and pouring pesticides. Some pesticides will have statements on their labels requiring the use of a specified respirator. Another means of inhalation exposure is smoking tobacco products containing pesticide residues. Toxicity Toxicity refers to the ability of a substance to produce adverse effects. These adverse effects may range from slight symptoms such as headaches to severe symptoms like coma, convulsions, or death. Poisons work by altering normal body functions. Most toxic effects are naturally reversible and do not cause permanent damage if prompt medical treatment is sought. Some poisons, however, cause irreversible (permanent) damage. Toxicity is usually divided into two types, acute or chronic, based on the number of exposures to a poison and the time it takes for toxic symptoms to develop. Acute toxicity is due to short-term exposure and happens within a relatively short period of time, whereas chronic exposure is due to repeated or long-term exposure and happens over a longer period. (Table 2). Table 2.

one week to years How Toxicity Is Measured All new pesticides are tested to establish the type of toxicity and the dose necessary to produce a measurable toxic reaction. In order to compare the results of toxicity tests done in different labs, there are strict testing procedures. Toxicity testing is extensive (involving many phases) and therefore expensive. Humans, obviously, cannot be used as test subjects, so toxicity testing is done with animals and plants. Since different species of animals respond differently to chemicals, a new chemical is generally tested in mice, rats, rabbits, and dogs. The results of these toxicity tests are used to predict the safety of the new chemical to humans. Toxicity tests are based on two premises. The first premise is that information about toxicity in animals can be used to predict toxicity in humans. Years of experience have shown that toxicity data obtained from a number of animal species can be useful in predicting human toxicity, while data obtained from a single species may be inaccurate. The second premise is that by exposing animals to large doses of a chemical for short periods of time, we can predict human toxicity from exposure to small doses for long periods of time. Both premises have been questioned. Chronic toxicity is tested using animal feeding studies.

In these studies, the pesticide under investigation is incorporated into the daily diet and fed to animals from a very young to a very old age. These, as well as the reproductive effects studies, are designed to arrive at a No-Observable-Effect-Level (NOEL); that is, a level in the total diet that causes no adverse effect in treated animals when compared to untreated animals maintained under identical conditions. This NOEL is expressed on a mg/kg of body weight/day basis. A Reference Dose (RfD), also known as Acceptable Daily Intake (ADD), is usually established at 1/100 of the NOEL, in order to add an additional margin of safety. The RfD (ADI) is the amount of chemical that can be consumed daily for a lifetime without ill effects. Acute Toxicity The acute toxicity of a chemical refers to its ability to do systemic damage as a result of a one-time exposure to relatively large amounts of the chemical. A pesticide with a high acute toxicity may be deadly if even a very small amount is absorbed. The signal words on the label (Table 3) are based on the acute toxicity of the pesticide.

Acute toxicity may be measured as acute oral (through the mouth), acute dermal (through the skin) and acute inhalation (through the lungs or respiratory system). Table 3. over one pint to one pound 1 Probable for a 150 lb.-person. Acute Toxicity Measures The commonly used term to describe acute toxicity is LD50. LD means lethal dose (deadly amount) and the subscript 50 means that the dose was acutely lethal to 50% of the animals to whom the chemical was administered under controlled laboratory conditions. The test animals are given specific amounts of the chemical in either one oral dose or by a single injection, and are then observed for a specified time. The lower the LD50 value, the more acutely toxic the pesticide. Therefore, a pesticide with an oral LD50 of 500 mg/kg would be much less toxic than a pesticide with an LD50 of 5 mg/kg. LD50 values are expressed as milligrams per kilogram (mg/kg), which means milligrams of chemical per kilogram of body weight of the animal. Milligram (mg) and kilogram (kg) are metric units of weight.

Milligrams per kilogram is the same measure as parts per million. To put these units into perspective, 1 ppm is analogous to 1 inch in 16 miles or 1 minute in 2 years. For example, if the oral LD50 of the insecticide parathion is 4 mg/kg, a dose of 4 parts of parathion for every million parts of body weight would be lethal to at least half of the test animals. LD50 values are generally expressed on the basis of active ingredient. If a commercial product is formulated to contain 50 percent active ingredient, it would take two parts of the material to make one part of the active ingredient. In some cases, other chemicals mixed with the active ingredient for formulating the pesticide product may cause the toxicity to differ from that of the active ingredient alone. Acute inhalation toxicity is measured by LC50. LC means lethal concentration. Concentration is used instead of dose because the amount of pesticide inhaled in the air is being measured. LC50 values are measured in milligrams per liter. Liters are metric units of volume similar to a quart. The lower the LC50 value, the more poisonous the pesticide.

Chronic Toxicity Chronic toxicity refers to harmful effects produced by long-term exposure to pesticides. Less is known about the chronic toxicity of pesticides than is known about their acute toxicity, not because it is of less importance, but because chronic toxicity is gradual rather than immediate and is revealed in much more complex and subtle ways. While situations resulting in acute exposure (a single large exposure) do occur, they are nearly always the result of an accident or careless handling. On the other hand, persons may be routinely exposed to pesticides while mixing, loading, and applying pesticides or by working in fields after pesticides have been applied. Chronic Toxicity Measures There is no standard measure like the LD50 for chronic toxicity. How chronic toxicity of chemicals is studied depends upon the adverse effect being studied. Chronic adverse effects may include carcinogenic effects (cancers), teratogenic effects (birth defects), mutagenic effects (genetic mutations), hemotoxic effects (blood disorders), endocrine disruption (hormonal problems), and reproductive toxicity (infertility or sterility). Carcinogenesis (oncogenesis) Carcinogenesis means the production of malignant tumors. Oncogenesis is a generic term meaning the production of tumors which may or may not be carcinogenic.

The terms tumor, cancer, or neoplasm are all used to mean an uncontrolled progressive growth of cells. In medical terminology, a cancer is considered a malignant (potentially lethal) neoplasm. Carcinogenic or oncogenic substances are substances that can cause the production of tumors. Examples are asbestos and cigarette smoke. Teratogenesis Teratogenesis is the production of birth defects. A teratogen is anything that is capable of producing changes in the structure or function of an embryo or fetus exposed before birth. An example of a chemical teratogen is the drug thalidomide, which caused birth defects in children when their mothers used it during their pregnancies. Measles virus infection during pregnancy has teratogenic effects. Mutagenesis Mutagenesis is the production of changes in genetic structure. A mutagen is a substance that causes a genetic change. Many mutagenic substances are oncogenic, meaning they also produce tumors. Many oncogenic substances are also mutagens. Reproductive toxicity Some chemicals have effects on the fertility or reproductive rates of animals. Males or females can be affected. Label Identification of Acute and Chronic Toxicity To alert pesticide users to the acute toxicity of a pesticide, a signal word may appear on the label.

Four different categories are used (Table 3). Signal words are used to tell the user whether the chemical is highly toxic, moderately toxic, slightly toxic, or relatively non-toxic. These label warnings are based, for the most part, on the chemical's acute toxicity. For example, the acute oral and acute dermal toxicity of a pesticide may be in the slightly toxic category. But if the acute inhalation toxicity is in the highly toxic category, the pesticide label will have the signal words for a highly toxic pesticide. The degree of eye or skin irritation caused by the pesticide also influences the signal word. For chronic toxicity there is no comparable set of signal words like those used for acute toxicity. Instead, a statement identifying the specific chronic toxicity problem is sometimes used on the label. Such a statement might read "This product contains (name of chemical), which has been determined to cause tumors or birth defects in laboratory animals." Chronic toxicity warning statements may be accompanied by label directions to wear certain kinds of protective clothing when handling or working with the pesticide to minimize or eliminate exposure to the pesticide. It is important to read the label to look for signal words identifying the product's acute toxicity and for statements identifying any chronic toxicity problem.

A pesticide may be low in acute toxicity (signal word caution), but it may have a label statement identifying potential chronic toxicity. Safety Factors Extensive residue trials are conducted on crops to determine levels of the pesticide that remain in or on growing crops after treatment with the pesticide. These trials lead to the establishment of a tolerance for residues of the chemical on food commodities. A tolerance is the maximum allowable amount of the pesticide permitted in or on a specific food commodity at harvest. The directions for use found on the product label are written to assure that residues in food commodities are below the tolerance. The tolerance is set low enough to assure that even if someone ate only food items with residues of a given pesticide at the tolerance limit, there would still be a safety factor of at least 100 when compared to a level causing no observable effects in laboratory animals. This is, of course, a worst-case situation, since all crops on which the pesticide is registered for use would not be treated with the chemical, and in most cases residue levels would be well below the tolerance because pre-harvest intervals are almost invariably longer than the minimum period stated on the label. Further reduction of residues may occur in storage or from washing, trimming, and processing.

Dose-response Dose-response is the measure of the amount of a given substance an organism must absorb to produce an effect. The extensive amount of data developed about a given pesticide is often used against it because this key piece of information is ignored. For example, some acute toxicity studies, which are designed to include dosage levels high enough to produce deaths, are cited as proof of the chemical's dangers. Chronic effects seen at very high doses in lifetime feeding studies are misinterpreted and considered as proof that no exposure to the chemical should be allowed. Major improvements in analytical chemistry permit detection of the presence of chemicals at extremely low levels of parts per billion (ppb) and even sometimes parts per trillion (ppt). A certain chemical may have been found in a food or beverage, and the amount found is expressed in parts per million or parts per billion. Often, no information is provided to assist consumers in comprehending the meaning of these numbers. Frequently, this information neglects the issue of dose-response, the key principle of toxicology, which, simply stated, is "the dose makes the poison." The concentration of a chemical in any substance is meaningless unless it is related to the toxicity of the chemical and the potential for exposure and absorption.

Chemicals of low toxicity such as table salt or ethyl alcohol can be fatal if consumed in large amounts. Conversely a highly toxic material may pose no hazard when exposure is minimal. Monitoring for Residues Monitoring foods for pesticide residues is carried out by the Food and Drug Administration (FDA) and the United States Department of Agriculture (USDA). Crops found to contain residues over the official tolerance (maximum legal level) established by the EPA must be destroyed. The threat of crop destruction with resultant financial loss is a strong incentive for farmers to observe use instructions on pesticide labels and thus assures that residues will be below established tolerances. Crops grown for export are often checked for residues by foreign residue laboratories to assure that local tolerance limits are not exceeded. Lastly, market-basket surveys (analyses of food items from grocery stores) have confirmed the low exposure of the general public to pesticides in foods. Hazard Hazard is a function of the toxicity of a pesticide and the potential for exposure to it. We do not have control of the toxicity of a pesticide because toxicity is a given characteristic of a particular pesticide; however, we can have control over our exposure to pesticides.

We achieve control over exposure by following several safety practices including the use of protective clothing and equipment (PPE). All pesticides are hazardous if misused, no matter what their toxicity. All pesticides can be handled safely by using safety practices that minimize or eliminate exposure to them. Federal laws regulating pesticides have placed the burden of proving safety of pesticide usage on the manufacturer. Hazard evaluation studies are generally done by scientific laboratories maintained by the manufacturer or through outside contract laboratories. Few products are subjected to the extensive and vigorous testing pesticides undergo before they are marketed. In fact, many promising pesticide products are not marketed because they do not pass the extensive toxicology testing. Older pesticide products that were registered before the current toxicology testing standards were established are being re-evaluated to ensure they meet current standards. Precautions and other safety information found on the product's label are based on information from these tests. By reading and following the directions on the label, users can minimize or eliminate hazards due to use of the pesticide to themselves and others. Common Pesticide Poisonings The pesticides most often implicated in poisonings, injuries, and illnesses, according to 2010 data from the American Association of Poison Control Center's Toxic Exposure Surveillance System, are listed in Table 4.

Cases listed as organophosphates (and the other categories as well) may also include other insecticides such as carbamates and organochlorine in a single product. Asymptomatic cases are included in Table 4 only. This list can't be considered representative of all symptomatic poisonings because it only shows cases reported to Poison Control Centers. However, it does give a sense of the relative frequency and risk of poisoning from various agents or classes of agents. The relative frequency of cases generally reflects how widely a product is used in the environment. For example, a number of disinfectants occur in the top ten partly because they are far more commonly found in the home and work environment than other pesticides. Denominator information on the population at risk (numbers exposed) would be needed to better understand the relative risk of different pesticides. However, the main purpose is to give physicians a sense of what types of cases they are most likely to see in their practice. Table 4.

109,495 Additional Information Some of the preceding material was adapted from Pesticide Toxicities, Leaflet 21062, Division of Agricultural Sciences, University of California and the Dose Makes the Poison by Alice Ottoboni, Ph.D., Vincente Books. Fishel, F.M. 2005. Evaluation of pesticides for carcinogenic potential. UF/IFAS EDIS Publication PI-37. . Visited January 2014. National Pesticide Information Center (1-800-858-7378 or ). Visited January 2014. Poison Information Center Network (1-800-222-1222 or ). Visited January 2014. Footnotes 1. This document is PI-13, one of a series of the Agronomy Department, UF/IFAS Extension. Original publication date July 1993. Revised January 2014. Reviewed January 2014. Visit the EDIS website at . 2. O. Norman Nesheim, Ph.D., professor emeritus, Food Science and Human Nutrition Department; Frederick M.

Fishel, professor, Agronomy Department, and Director, Pesticide Information Office; and Mark Mossler, Doctor of Plant Medicine, Agronomy Department; UF/IFAS Extension, Gainesville, FL 32611. Use pesticides safely. Read and follow directions on the manufacturer's label. The Institute of Food and Agricultural Sciences (IFAS) is an Equal Opportunity Institution authorized to provide research, educational information and other services only to individuals and institutions that function with non-discrimination with respect to race, creed, color, religion, age, disability, sex, sexual orientation, marital status, national origin, political opinions or affiliations. For more information on obtaining other UF/IFAS Extension publications, contact your county's UF/IFAS Extension office. U.S. Department of Agriculture, UF/IFAS Extension Service, University of Florida, IFAS, Florida A & M University Cooperative Extension Program, and Boards of County Commissioners Cooperating. Nick T. Place, dean for UF/IFAS Extension. Lead (Pb) Toxicity: What Are the Physiologic Effects of Lead Exposure?

| ATSDR - Environmental Medicine & Environmental Health Education - CSEM reduced IQ scores weakness There is also some evidence that lead exposure may affect adults' postural balance and peripheral nerve function. (ATSDR 1997a, b; Arnvig et al. 1980; Haenninen et al. 1978; Hogstedt et al. 1983; Mantere et al. 1982; Valciukas et al. 1978 as cited in ATSDR 1999) Slowed nerve conduction and forearm extensor weakness (wrist drop), as late signs of lead intoxication, are more classic signs in workers chronically exposed to high lead levels Renal Effects Many studies show a strong association between lead exposure and renal effects. (ATSDR 1999) Acute high dose lead-induced impairment of proximal tubular function manifests in aminoaciduria, glycosuria, and hyperphosphaturia (a Fanconi-like syndrome). These effects appear to be reversible (ATSDR 1999).

However, continued or repetitive exposures can cause a toxic stress on the kidney, if unrelieved, may develop into chronic and often irreversible lead nephropathy (i.e., chronic interstitial nephritis). The lowest level at which lead has an adverse effect on the kidney remains unknown. Most documented renal effects for occupational workers have been observed in acute high-dose exposures and high-to-moderate chronic exposures (BLL > 60 µg/dL). Currently, there are no early and sensitive indicators (e.g., biomarkers) considered predictive or indicative of renal damage from lead. (ATSDR 2000) Serum creatinine and creatinine clearance are used as later indicators. However, certain urinary biomarkers of the proximal tubule (e.g., NAG) show elevations with current exposures, even at BLLs less than 60 µg/dL; and some population-based studies show accelerated increases in serum creatinine or decrements in creatinine clearance at BLLs below 60 µg/dL. (Staessen et al. 1992; Kim et al. 1996; Payton et al. 1994; Tsaih et al.

2004) Latent effects of lead exposure that occurred years earlier in childhood may cause some chronic advanced renal disease or decrement in renal function. In children, the acute lead-induced renal effects appear reversible with recovery usually occurring within two months of treatment. (Chisolm et al. 1976) Treatment of acute lead nephropathy in children appears to prevent the progression to chronic interstitial nephritis. (Weeden et al. 1986) It should be noted that lead-induced end-stage renal disease is a relatively rare occurrence in the U.S. population. Renal disease can be asymptomatic until the late stages and may not be detected unless tests are performed. Because past or ongoing excessive lead exposure may also be a causative agent in kidney disease associated with essential hypertension (ATSDR 1999), primary care providers should follow closely the renal function of patients with hypertension and a history of lead exposure. (See “Hypertension Effects” section). Lead exposure is also believed to contribute to “saturnine gout,” which may develop because of lead-induced hyperuricemia due to decreased renal excretion of uric acid.

In one study, more than 50% of patients suffering from lead nephropathy also suffered from gout. (Bennett 1985 as cited in ATSDR 2000) Saturnine gout is characterized by less frequent attacks than primary gout. Lead-associated gout may occur in pre-menopausal women, an uncommon occurrence in non lead-associated gout. (Goyer 1985, as cited in ATSDR 2000) A study by Batuman et al (1981) suggests that renal disease is more frequent and more severe in saturnine gout than in primary gout. Hematological Effects Lead inhibits the body's ability to make hemoglobin by interfering with several enzymatic steps in the heme pathway. Specifically, lead decreases heme biosynthesis by inhibiting d-aminolevulinic acid dehydratase (ALAD) and ferrochelatase activity. Ferrochelatase, which catalyzes the insertion of iron into protoporphyrin IX, is quite sensitive to lead.

A decrease in the activity of this enzyme results in an increase of the substrate, erythrocyte protoporphyrin (EP), in the red blood cells (also found in the form of ZPP—bound to zinc rather than to iron). Also associated with lead exposure is an increase in blood and plasma d-aminolevulinic acid (ALA) and free erythrocyte protoporphyrins (FEP) (EPA 1986a as cited in ATSDR 1999). EPA estimated the threshold BLL for a decrease in hemoglobin to be 50 µg/dL for occupationally exposed adults and approximately 40 µg/dL for children, although other studies have indicated a lower threshold (e.g., 25 µg/dL) for children.

(EPA 1986b as cited in ATSDR 1999; ATSDR 1999) Recent data indicate that the EP level, which has been used in the past to screen for lead toxicity, is not sufficiently sensitive at lower levels of blood lead and is therefore not as useful a screening test as previously thought (see the “Laboratory Evaluation” section for further discussion of EP testing.). Lead can induce two types of anemia, often accompanied by basophilic stippling of the erythrocytes. (ATSDR 1999) Acute high-level lead exposure has been associated with hemolytic anemia. Frank anemia is not an early manifestation of lead exposure and is evident only when the BLL is significantly elevated for prolonged periods. In chronic lead exposure, lead induces anemia by both interfering with heme biosynthesis and by diminishing red blood cell survival. The anemia of lead intoxication is hypochromic, and normo- or microcytic with associated reticulocytosis. The heme synthesis pathway, on which lead has an effect, is involved in many other processes in the body including neural, renal, endocrine, and hepatic pathways.

There is a concern about the meaning of and possible sequelae of these biochemical and enzyme changes at lower levels of lead. Endocrine Effects Studies of children with high lead exposure have found that a strong inverse correlation exists between BLLs and vitamin D levels. Lead impedes vitamin D conversion into its hormonal form, 1, 25-dihydroxyvitamin D, which is largely responsible for the maintenance of extra- and intra-cellular calcium homeostasis. Diminished 1, 25-dihydroxyvitamin D, in turn, may impair cell growth, maturation, and tooth and bone development. In general, these adverse effects seem to be restricted to children with chronically high BLLs (most striking in children with BLLs > 62 µg/dL) and chronic nutritional deficiency, especially with regard to calcium, phosphorous, and vitamin D (Koo et al. 1991 as cited in ATSDR 1999). However, Rosen et al.

(1980) noted that in lead-exposed children with blood lead levels of 33-55 µg/dL, 1, 25-dihydroxyvitamin D levels were reduced to levels comparable to those observed in children with severe renal insufficiency. Lead appears to have a minimal, if any, effect on thyroid function. Gastrointestinal Effects In severe cases of lead poisoning, children or adults may present with severe cramping abdominal pain, which may be mistaken for an acute abdomen or appendicitis. Cardiovascular (Hypertension) Effects Hypertension is a complex condition with many different causes and risk factors, including age, weight, diet, and exercise habits. Lead exposure is one factor of many that may contribute to the onset and development of hypertension. Although low to moderate lead level exposures (BLL<30 µg/dL) show only a low degree of association with hypertension, higher exposures (primarily occupational) increase the risk for hypertensive heart disease and cerebrovascular disease as latent effects. One study found that adults who experienced lead poisoning as children had a significantly higher risk of hypertension 50 years later (relative to control adults without childhood lead exposure).

(Hu, 1991, as cited in ATSDR 2000) The association has been shown in population-based studies with BLLs below 10 µg/dL. Data supports an association between lead exposure and elevations in blood pressure. (Victery et al. 1988; Schwartz 1995 as cited in ATSDR 2000; Korrick et al. 1999; Hu et al. 1996) It is estimated that, on a population basis, blood lead can account for a 1% to 2% variance in blood pressure. (ATSDR 2000) This could increase the incidence of hypertension a substantial amount, due to the high prevalence of hypertension of all causes in general populations. Reproductive Effects Reproductive effects examined in the literature include sperm count, fertility, and pregnancy outcomes. While several studies have implicated lead as contributing to reproductive and developmental effects, these effects have not been well-established at low exposure levels. Male Reproductive Effects Recent reproductive function studies in humans suggest that current occupational exposures decrease sperm count totals and increase abnormal sperm frequencies (Alexander et al. 1996; Gennart et al.

1992; Lerda 1992; and Lin et al. 1996 as cited in ATSDR 2000; Telisman et al. 2000). Effects may begin at BLLs of 40 µg/dL. (ATSDR 2005) Long-term lead exposure (independent of current lead exposure levels) also may diminish sperm concentrations, total sperm counts, and total sperm motility (Alexander et al. 1996 as cited in ATSDR 2000). It is unclear how long these effects may last in humans after lead exposure ceases. Fertility It is not currently possible to predict fertility outcomes based on current BLLs or past lead exposure levels. (ATSDR 2000) Pregnancy Outcomes The effect of low-level lead exposures on pregnancy outcomes is not clear. Thus it appears that at higher (e.g., occupational) exposure levels, the evidence is clearer for an association between lead and adverse pregnancy outcomes. This association becomes equivocal when looking at women exposed to lower environmental levels of lead. The data concerning exposure levels are incomplete, probably a result of far greater exposures than are currently found in lead industries.

Some studies of women living near smelters versus those living some distance away did show increased frequency of spontaneous abortions (Nordstrom et al. 1979) and miscarriages and stillbirths (Baghurst et al. 1987; McMichael et al. 1986). In contrast, Murphy et al. (1990) evaluated past pregnancy outcomes among women living in the vicinity of a lead smelter and did not find an increase in spontaneous abortion risk among the lead exposed group versus the unexposed group. Women with BLL 5-9 µg/dL were two to three times more likely to have a spontaneous abortion than were women with BLL lesser than 5 µg/dL. (Borja-Aburto et al. 1999). Developmental Effects Developmental effects examined in the literature include pregnancy outcomes (e.g., premature births and low birth weights), congenital abnormalities, and post birth effects on growth or neurological development. Increasing evidence indicates that lead, which readily crosses the placenta, adversely affects fetus viability as well as fetal and early childhood development.

Prenatal exposure to low lead levels (e.g., maternal BLLs of 14 µg/dL) may increase the risk of reduced birth weight and premature birth (ATSDR 1999). Although lead is an animal teratogen, most human studies have not shown a relationship between lead levels and congenital malformations. A study by Needleman et al. (1984) correlated increased prenatal lead exposure with increased risk for minor congenital abnormalities (e.g., minor skin abnormalities and undescended testicles). No association between prenatal lead exposure and major congenital abnormalities has been found (Ernhart et al. 1985, 1986; McMichael et al. 1986). In a retrospective study, a higher proportion of learning disabilities were found among school-aged children with biological parents who were lead poisoned as children 50 years previously (Hu 1991). Other Potential Effects Lead has been linked to problems with the development and health of bones. At high levels, lead can result in slowed growth in children. Studies have shown increased likelihood of osteoporosis (weakened bones later in life) in animals exposed to lead.

A review of this issue can be found in Puzas (1992). Although this link has not been established in humans, it is likely that upon closer examination of lead-exposed individuals, lead will be shown to be a new risk factor for the disease. Research currently underway may provide more information about potential impacts of lead on osteoporosis (bone health) in the future. Current available data are not sufficient to determine the carcinogenicity of lead in humans. EPA has classified elemental lead and inorganic lead compounds as Group 2B: probable human carcinogens. (ATSDR 1999) This classification is based in part on animal studies, which have been criticized because the doses of lead administered were extremely high (ATSDR 1999). The National Toxicology Program classifies lead and lead compounds as “reasonably anticipated to be a carcinogen” (NTP 2004). Information regarding the association of occupational exposure to lead with increased cancer risk is generally limited.

This is because these occupational exposure studies, which primarily examined lead smelters, involved confounding exposures to other chemicals, including arsenic, cadmium, antimony, and toxicants from worker smoking habits (Cooper 1976 and IARC 1987). Researchers are currently investigating the impacts of lead on dental health. One study found pre- and perinatal exposure to lead increased prevalence of caries in rat pups by almost 40% (Watson 1997). Human epidemiological studies suggesting an association between lead exposure and caries although this has not been well-established (Bowen 2001). Key Points Effects in children generally occur at lower BLLs than in adults. The developing nervous system of a child can be affected adversely at BLLs of less than 10 µg/dL. It is often impossible to determine these effects upon clinical examination. There is a wide range of neurological effects associated with lead exposure, some of which may likely be irreversible. Lead exposure can lead to renal effects such as Fanconi-like syndromes, chronic nephropathy, and gout.

Most lead-associated renal effects or disease are a result of ongoing chronic or present high acute exposure or can be a latent effect of chronic past lead exposure. Lead inhibits several enzymes critical to the synthesis of heme, causing a decrease in blood hemoglobin. Today, lead exposure in children only rarely results in frank anemia. Lead's impairment of heme synthesis can affect other heme-dependent processes in the body outside of the hematopoietic system. Lead interferes with a hormonal form of vitamin D, which affects multiple processes in the body, including cell maturation and skeletal growth. Lead exposure may lead to increased risk for hypertension and its sequelae. Evidence suggests an association between lead exposure and certain reproductive and developmental outcomes. Maternal blood lead, from exogenous and endogenous sources, can cross the placenta and put the fetus at risk. Other potential health effects of lead are currently being studied. Definition of Lead poisoning Our Lead Poisoning Main Article provides a comprehensive look at the who, what, when and how of Lead Poisoning Definition of Lead poisoning First Aid Sprains & Strains Slideshow Pictures Lead poisoning: An acute or chronic poisoning caused by the absorption of lead or any of its salts into the body.

Lead poisoning is an environmental hazard that is capable of causing mental retardation, behavioral disturbance, and brain damage. Lead poisoning is formally defined in the US as at least 10 micrograms of lead per deciliter of blood. Lead poisoning is more common in children than in adults because young children often put their hands and other objects in their mouths, and these objects can have lead dust on them. Furthermore, lead poisoning is more dangerous in children than in adults because children absorb more lead and the developing brain and nervous system are more sensitive to the damaging effects of lead. Lead was used in household paint until 1978, and it was also found in leaded gasoline, some types of batteries, water pipes, and pottery glazes. Lead paint and pipes are still found in many older homes, and lead is sometimes also found in water, food, household dust, and soil. Lead can be a workplace hazard for people in some occupations. A diet that is high in iron and calcium can help protect people against absorbing lead. Treatment involves chelation therapy, whereby blood is removed and metals are filtered out through a machine, then reinfused into the patient. Treatment cannot repair damage to the brain done by lead poisoning, but it may prevent further damage.

Also known as plumbism. Last Editorial Review: 5/13/2016

Question: In humans, plumbism is chronic poisoning due to the absorption of what into the body?
Answer: Lead